Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1(-/y) mice.
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Altered Neuronal and Circuit Excitability in Fragile X Syndrome.Targeted pharmacological treatment of autism spectrum disorders: fragile X and Rett syndromesFragile X mental retardation protein regulates olfactory sensitivity but not odorant discriminationThe sodium-activated potassium channel Slack is required for optimal cognitive flexibility in miceStructural-functional connectivity deficits of neocortical circuits in the Fmr1 (-/y) mouse model of autism.Therapeutic Strategies in Fragile X Syndrome: From Bench to Bedside and BackSensory processing in autism spectrum disorders and Fragile X syndrome-From the clinic to animal models.BK Channels in the Central Nervous System.Strings on a Violin: Location Dependence of Frequency Tuning in Active DendritesReduced Inhibition within Layer IV of Sert Knockout Rat Barrel Cortex is Associated with Faster Sensory Integration.Multiple Sensory Inputs Are Extensively Integrated to Modulate Nociception in C. elegans.Fmr1 deficiency promotes age-dependent alterations in the cortical synaptic proteome.Metabotropic glutamate receptor 5 responses dictate differentiation of neural progenitors to NMDA-responsive cells in fragile X syndrome.The Shaping of Two Distinct Dendritic Spikes by A-Type Voltage-Gated K(+) ChannelsElevated CaMKIIα and Hyperphosphorylation of Homer Mediate Circuit Dysfunction in a Fragile X Syndrome Mouse Model.Moving Toward Integrative, Multidimensional Research in Modern Psychiatry: Lessons Learned From Fragile X SyndromeSensory hypo-excitability in a rat model of fetal development in Fragile X Syndrome.The utility of rodent models of autism spectrum disordersTreatment Approaches in Rodent Models for Autism Spectrum Disorder.Behavioral abnormalities in the Fmr1-KO2 mouse model of fragile X syndrome: The relevance of early life phases.Neuron class-specific requirements for Fragile X Mental Retardation Protein in critical period development of calcium signaling in learning and memory circuitry.Disrupted Cortical State Regulation in a Rat Model of Fragile X Syndrome.Increased Persistent Sodium Current Causes Neuronal Hyperexcitability in the Entorhinal Cortex of Fmr1 Knockout Mice.Cell-Type Specific Channelopathies in the Prefrontal Cortex of the fmr1-/y Mouse Model of Fragile X Syndrome.Reduced Lateral Inhibition Impairs Olfactory Computations and Behaviors in a Drosophila Model of Fragile X Syndrome.Excitability is increased in hippocampal CA1 pyramidal cells of Fmr1 knockout mice.Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice.Tactile Defensiveness and Impaired Adaptation of Neuronal Activity in the Fmr1 Knock-Out Mouse Model of Autism.Genetic Reduction of Matrix Metalloproteinase-9 Promotes Formation of Perineuronal Nets Around Parvalbumin-Expressing Interneurons and Normalizes Auditory Cortex Responses in Developing Fmr1 Knock-Out Mice.Identifying specific prefrontal neurons that contribute to autism-associated abnormalities in physiology and social behavior.Delayed in vitro development of Up states but normal network plasticity in Fragile X circuits.Aberrant Rac1-cofilin signaling mediates defects in dendritic spines, synaptic function, and sensory perception in fragile X syndrome.Delayed Maturation of Fast-Spiking Interneurons Is Rectified by Activation of the TrkB Receptor in the Mouse Model of Fragile X Syndrome.Increased transient Na+ conductance and action potential output in layer 2/3 prefrontal cortex neurons of the fmr1-/y mouse.Auditory repetition suppression alterations in relation to cognitive functioning in fragile X syndrome: a combined EEG and machine learning approach.Potential Involvement of Impaired BKCa Channel Function in Sensory Defensiveness and Some Behavioral Disturbances Induced by Unfamiliar Environment in a Mouse Model of Fragile X Syndrome.Functional changes of AMPA responses in human induced pluripotent stem cell-derived neural progenitors in fragile X syndrome.Genetic upregulation of BK channel activity normalizes multiple synaptic and circuit defects in a mouse model of fragile X syndrome.Neural Circuits: Reduced Inhibition in Fragile X Syndrome.Of Men and Mice: Modeling the Fragile X Syndrome.
P2860
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P2860
Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1(-/y) mice.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年学术文章
@wuu
2014年学术文章
@zh
2014年学术文章
@zh-cn
2014年学术文章
@zh-hans
2014年学术文章
@zh-my
2014年学术文章
@zh-sg
2014年學術文章
@yue
2014年學術文章
@zh-hant
name
Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1
@nl
Dendritic channelopathies cont ...... xcitability in Fmr1(-/y) mice.
@en
type
label
Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1
@nl
Dendritic channelopathies cont ...... xcitability in Fmr1(-/y) mice.
@en
prefLabel
Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1
@nl
Dendritic channelopathies cont ...... xcitability in Fmr1(-/y) mice.
@en
P2093
P2860
P356
P1433
P1476
Dendritic channelopathies cont ...... excitability in Fmr1(-/y) mice
@en
P2093
Andreas Frick
Audrey Bonnan
Ben Oostra
Guillaume Bony
Gwen LeMasson
Jean Rossier
Melanie Ginger
Nathalie Sans
Susanna Pietropaolo
P2860
P2888
P304
P356
10.1038/NN.3864
P407
P577
2014-11-10T00:00:00Z